Ischemic Heart Disease

Question 1

What is the result of IHD?

Answer 1

imbalance between cardiac blood supply

& myocardial oxygen & nutritional requirements

Question 2

What does ischemia result to?

Answer 2

• > 90% of cases reduction in coronary blood flow due to atherosclerosis – coronary artery disease (CAD)
• Increased demand ( heart rate or HTN)
• Blood volume (hypotension or shock)
• oxygenation (pneumonia or CHF)
• Diminished oxygen-carrying capacity (anemia & CO poisoning)

Question 3

• Severity or duration of ischemia causes_______

Answer 3

ACUTE MYOCARDIAL INFARCTION (MI)

Question 4

How does sudden cardiac result to?

Answer 4

• Due to tissue damage from MI but most commonly from a

lethal arrhythmia without myocyte necrosis following MI.

Question 5

Name the three acute coronary syndrome

Answer 5

• Unstable angina
• Acute MI
• SCD

Question 6

What are the three coronary arteries that results in artherosclerotic narrowing?

Answer 6

1. Left anterior descending artery (LAD)
2. Left circumflex artery (LCX)
3. Right coronary artery (RCA)

Question 7

What happens if a lesion obstructs > 70% of a vessel lumen (critical
stenosis) ?

Answer 7

It causes angina only during increased demand

stable angina

Question 8

What happens in Fixed ≥ 90% stenosis?

Answer 8

angina at rest (unstable

angina)

Question 9

Slowly progressive atherosclerotic occlusion leads to___________

Answer 9

the establishment of collateral blood flow

Question 10

What is the Role of inflammation?

Answer 10

• From inception to plaque rupture

Question 11

What happens if the lumen diameter decreases?

Answer 11

leads to increase local mechanical stress and leads to plaque disruption

Question 12

How is vasoconstriction stimulated?

Answer 12

1. Circulating adrenergic agonists
2. Locally released platelet contents
3. Imbalance between EC relaxants (NO) & constrictors
   (endothelin)
4. Mediators released from perivascular inflammatory
   cells

Question 13

How does Acute Plaque Change occur?

Answer 13

• Rupture, fissuring or ulceration of plaque

- Hemorrhage into the core of plaque

Question 14

What are Vulnerable plaques?

Answer 14

– having large atheromatous cores or thin fibrous caps

Question 15

What is the Location of fissures

Answer 15

junction of fibrous cap & adjacent normal arterial segment

Question 16

Adrenergic stimulation can elevate physical stresses on the plaque through_________

Answer 16

systemic HTN or local vasospasm

Question 17

What leads to plaque

enlargement

Answer 17

Healing of subclinical plaque disruption

& overlying thrombosis

Question 18

What is angina pectoris

Answer 18

•Intermittent chest pain caused by

transient, reversible myocardial ischemia

Question 19

What is Typical or stable angina?

Answer 19

• Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand e.g.,
tachycardia due to fever, anxiety & fear

Question 20

What is Prinzmetal or variant angina?

Answer 20

• Angina occurring at rest due to coronary artery spasm

• Prompt response to the administration of vasodilators such as
nitroglycerin or calcium channel blockers

Question 21

What is Unstable angina (crescendo angina)?

Answer 21

•Increasing frequency of pain, precipitated by progressively
less exertion or even occurring at rest
• Episodes also tend to be more intense & longer lasting than
stable angina

Question 22

Unstable angina is associated with?

Answer 22

Plaque disruption & superimposed partial thrombosis
Distal embolization of thrombus and vasospasm
Pre-infarction angina

Question 23

Define Myocardial Infarction?

Answer 23

•Necrosis of heart muscle resulting from ischemia

Question 24

MI’s are caused by_________

Answer 24

acute coronary artery thrombosis

Question 25

Occasionally severe diffuse coronary ATH causes________

Answer 25

subendocardial infarction

Question 26

Name some examples of

Disorders of small intramyocardial arterioles

Answer 26

vasculitis,

amyloid deposition or stasis

Question 27

What are the biochemical consequences seen in the MI?

Answer 27

• Within seconds cardiac myocyte aerobic glycolysis ceases

and leads to decreased ATP production & accumulation of lactic acid

Question 28

What are the functional consequences seen in the MI?

Answer 28

• Loss of contractility occurs within a minute

Question 29

How is transmural infarcts caused ?

Answer 29

Caused by epicardial vessel occlusion through a combination of
Chronic atherosclerosis & acute thrombosis
- ECG leads to ST segment elevation
- Also called ST segment elevated MIs (STEMIs)

Question 30

What are the causes of Subendocardial infarcts?

Answer 30

1. Severe coronary artery disease (CAD)
2. Transient decrease in oxygen delivery (hypotension, anemia)
3. Increased oxygen demand (tachycardia, HTN)
4. Thrombolysis before the development of a full-thickness infarct

Question 31

What are microscopic infarcts?

Answer 31

• Small vessel occlusions

- Vasculitis, embolization of valve vegetations or mural thrombi or vessel spasm due to increased catecholamines

Question 32

What does Mitochondrial dysfunction leads to

Answer 32

apoptosis

Question 33

What does Myocyte hypercontracture leads to?

Answer 33

: increased cytosolic Ca due to ischemia – REPERFUSION leads to augmented contraction leads to cytoskeletal damage & cell death

Question 34

What does Free radical generation leads to?

Answer 34

membrane protein &

phospholipid damage

Question 35

What does Leukocyte aggregation lead to?

Answer 35

no-reflow phenomenon,

elaboration of proteases & elastases

Question 36

What is the ECG abnormalities seen in MI?

Answer 36

• Q wave – indicative of transmural infarcts
• ST-segment abnormalities
• T-wave inversion